Breathing during exercise is precisely controlled to maintain arterial PCO2 at resting, control levels. Known CO2 sensitive receptors require an error signal in PaCO2 above the resting level in order to increase ventilation. Certain theories of ventilatory control suggest that the rate of CO2 delivery to the lungs is the key parameter which is driving breathing. This CO2 flux theory of ventilatry control suffers from the lack of known receptors capable of sensing CO2 flow to the lungs. Birds on the other hand are known to possess intrapulmonary CO2 receptors (IPC). Previous work (Tallman et al. l979) has shown that these receptors can affect the duration of inspiration and expiration in a breath-by-breath manner somewhat similar to the mammalian Hering-Breuer reflex. The proposed research will test the CO2 flux theory in these animals by determining whether the intrapulmonary CO2 receptors are capable of adjusting ventilation to match changes in the rate of carbon dioxide delivery to the lungs. Experiments will be conducted on decerebrate Pekin ducks. A veno-venous extracorporeal blood circuit with a silicone membrane blood oxgyenator will be used to change the PCO2 of the venous blood, thus altering the CO2 flux to the lungs. Ventilatory and arterial blood gas responses to changes in CO2 flux will be compared to those responses measured during inspired CO2 loading. Denervation of the arterial chemoreceptors will then be performed and the experiments repeated to better evaluate the role played by the lung receptors in the observed responses. Single unit recording of IPC discharge will also be made to determine how these receptors might be affected by different levels of CO2 delivery to the lungs. The dynamics of the ventilatory response to both methods of CO2 loading will also be studied. These experiments will contribute greatly to our understanding of exercise hyperpnea by demonstrating if and how, lung CO2 sensitive receptors are involved in the regulation of arterial levels of endogenously produced CO2.